Evidence map›Paper›PMID 41385922›Full record

SynthesisInternational dental journal2026

Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta.

Tina Leban, Tanja Kunej

Abstract readSystematic Review
In one paragraph

Synthesis in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Integrative multi-omics and bioinformatic analysis ofThe Japanese dental science review · 2026
    Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Tina LebanFaculty of Medicine, Department of Paediatric and Preventive Dentistry, University of Ljubljana, Ljubljana, Slovenia. Electronic address: tina.leban@mf.uni-lj.si.
Tanja KunejBiotechnical Faculty, Department of Animal Science, University of Ljubljana, Ljubljana, Slovenia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesFAM83H is a critical gene implicated in amelogenesis imperfecta type IIIA (AI type IIIA), but its precise role in enamel formation remains poorly understood. Fragmented datasets, inconsistent terminology, and limited integrative analyses hinder functional interpretation. This study presents a comprehensive multi-omics analysis of FAM83H-associated AI type IIIA.

methodsA systematic literature search (February 2008-June 2025) was conducted in PubMed and Web of Science using targeted keywords spanning genomics, transcriptomics, epigenomics, miRNomics, proteomics, interactomics, epiproteomics, metabolomics, glycomics, lipidomics, intracellular localization, phenomics, pharmacogenomics, and environmental omics. Data were extracted using 13 bioinformatic tools and databases including Ensembl, ENCODE, OMIM, HGNC, HGMD, dbSNP, gnomAD, miRBase, TargetScanHuman, MethPrimer, dbPTM, STRING, and MalaCards.

resultsOf 150 screened publications, 62 met the inclusion criteria and were categorized across 12 omics layers. Key findings, derived from both published studies and bioinformatic databases/tools, include 38 single nucleotide polymorphisms (SNPs), two CpG islands, 932 predicted micro RNA (miRNA) binding sites, and multiple post-translational modifications. A protein-protein interaction network constructed from 18 AI-associated proteins, including FAM83H, revealed significant connectivity among enamel matrix-related proteins and provided a framework for exploring potential functional associations.

conclusionThis study presents a multi-omics regulatory atlas of FAM83H, encompassing genetic variants, epigenetic changes, and post-translational modifications that are predicted to influence its biological function and role in disease. CLINICAL RELEVANCE: The integrative methodology supports FAM83H as a model gene for elucidating the molecular mechanisms of amelogenesis imperfecta and may facilitate improved diagnosis and targeted therapeutic strategies for AI type IIIA.

Indexed as

Amelogenesis ImperfectaProteinsComputational BiologyGenomicsHumansMicroRNAsMultiomicsPolymorphism, Single NucleotideFAM83H protein, humanMicroRNAsProteinsAI type IIIAAmelogenesis imperfectaEnamel formationFAM83HHypomineralizationMulti-omics

Identifiers

PMID41385922
PMCPMC12757458

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.